Stellar winds from Massive Stars

We review the various techniques through which wind properties of massive stars - O stars, AB supergiants, Luminous Blue Variables (LBVs), Wolf-Rayet (WR) stars and cool supergiants - are derived. The wind momentum-luminosity relation (e.g. Kudritzki et al. 1999) provides a method of predicting mass-loss rates of O stars and blue supergiants which is superior to previous parameterizations. Assuming the theoretical sqrt(Z) metallicity dependence, Magellanic Cloud O star mass-loss rates are typically matched to within a factor of two for various calibrations. Stellar winds from LBVs are typically denser and slower than equivalent B supergiants, with exceptional mass-loss rates during giant eruptions Mdot=10^-3 .. 10^-1 Mo/yr (Drissen et al. 2001). Recent mass-loss rates for Galactic WR stars indicate a downward revision of 2-4 relative to previous calibrations due to clumping (e.g. Schmutz 1997), although evidence for a metallicity dependence remains inconclusive (Crowther 2000). Mass-loss properties of luminous (> 10^5 Lo) yellow and red supergiants from alternative techniques remain highly contradictory. Recent Galactic and LMC results for RSG reveal a large scatter such that typical mass-loss rates lie in the range 10^-6 .. 10^-4 Mo/yr, with a few cases exhibiting 10^-3 Mo/yr.Comment: 16 pages, 2 figures, Review paper to appear in Proc `The influence of binaries on stellar population studies', Brussels, Aug 2000 (D. Vanbeveren ed.), Kluwe

Mass loss from hot massive stars

Mass loss is a key process in the evolution of massive stars, and must be understood quantitatively to be successfully included in broader astrophysical applications. In this review, we discuss various aspects of radiation driven mass loss, both from the theoretical and the observational side. We focus on winds from OB-stars, with some excursions to the Luminous Blue Variables, Wolf- Rayet stars, A-supergiants and Central Stars of Planetary Nebulae. After reca- pitulating the 1-D, stationary standard model of line-driven wind, extensions accounting for rotation and magnetic fields are discussed. The relevance of the so-called bi-stability jump is outlined. We summarize diagnostical methods to infer wind properties from observations, and compare the results with theore- tical predictions, featuring the massloss-metallicity dependence. Subsequently, we concentrate on two urgent problems which challenge our present understanding of radiation driven winds: weak winds and wind- clumping. We discuss problems of measuring mass-loss rates from weak winds and the potential of NIR- spectroscopy. Wind-clumping has severe implications for the interpretation of observational diagnostics, as derived mass-loss rates can be overestimated by factors of 2 to 10 if clumping is ignored, and we describe ongoing attempts to allow for more uniform results. We point out that independent arguments from stellar evolution favor a moderate reduction of present- day mass-loss rates. We also consider larger scale wind structure, interpreted in terms of co-rotating interacting regions, and complete this review with a discussion of recent progress on the X-ray line emission from massive stars, highlighting as to how far the analysis of such X-ray line emission can give further clues regarding an adequate description of wind clumping. (Abridged abstract)Comment: Astronomy and Astrophysics Review (accepted

Loss of function mutation of the Slc38a3 glutamine transporter reveals its critical role for amino acid metabolism in the liver, brain, and kidney

Glutamine, the most abundant amino acid in mammals, is critical for cell and organ functions. Its metabolism depends on the ability of cells to take up or release glutamine by transporters located in the plasma membrane. Several solute carrier (SLC) families transport glutamine, but the SLC38 family has been thought to be mostly responsible for glutamine transport. We demonstrate that despite the large number of glutamine transporters, the loss of Snat3/Slc38a3 glutamine transporter has a major impact on the function of organs expressing it. Snat3 mutant mice were generated by N-ethyl-N-nitrosurea (ENU) mutagenesis and showed stunted growth, altered amino acid levels, hypoglycemia, and died around 20 days after birth. Hepatic concentrations of glutamine, glutamate, leucine, phenylalanine, and tryptophan were highly reduced paralleled by downregulation of the mTOR pathway possibly linking reduced amino acid availability to impaired growth and glucose homeostasis. Snat3-deficient mice had altered urea levels paralleled by dysregulation of the urea cycle, gluconeogenesis, and glutamine synthesis. Mice were ataxic with higher glutamine but reduced glutamate and gamma-aminobutyric acid (GABA) levels in brain consistent with a major role of Snat3 in the glutamine-glutamate cycle. Renal ammonium excretion was lower, and the expression of enzymes and amino acid transporters involved in ammoniagenesis were altered. Thus, SNAT3 is a glutamine transporter required for amino acid homeostasis and determines critical functions in various organs. Despite the large number of glutamine transporters, loss of Snat3 cannot be compensated, suggesting that this transporter is a major route of glutamine transport in the liver, brain, and kidney